MCL Literature Feed

Consensus guidelines recommend the BOVen triplet (zanubrutinib, obinutuzumab, venetoclax) for TP53-mutated MCL and CAR-T for BTKi-refractory disease, providing expert guidance for managing high-risk patients.

The novel BCL-2 inhibitor lisaftoclax demonstrated a 50% overall response rate and manageable safety in a phase 1 trial of Chinese patients with relapsed/refractory MCL.

This review provides a treatment and sequencing algorithm for relapsed/refractory MCL, navigating the complex landscape of BTKi, BCL2i, CAR-T, bispecifics, and transplant for individualized patient care.

This paper details a new UPLC-MS/MS method for rapid venetoclax plasma quantification, which could facilitate therapeutic drug monitoring to optimize dosing and toxicity management in MCL.

This review summarizes the shift towards frontline BTK inhibitor-based regimens, including chemotherapy-free options and combinations for high-risk MCL, potentially replacing autologous stem cell transplant consolidation.

This preclinical study shows a SOX11 inhibitor overcomes BTKi, BCL2i, and CAR-T resistance by targeting the PAX5/CD19 axis, a novel upstream BCR signaling mechanism.

This review of BCL-2 inhibitors in other indolent lymphomas provides context for their use in MCL, summarizing preclinical and clinical data supporting this therapeutic class in B-cell malignancies.

An albumin nanocomplex of the BCL-2/xL inhibitor APG-1252 reduces thrombocytopenia and enhances anti-MCL efficacy in mouse models, offering a potential strategy to improve the therapeutic window.

Long-term follow-up (37.2 months) in Japanese relapsed/refractory MCL patients shows the ibrutinib-venetoclax combination yields durable complete responses (83% CR), high MRD negativity, and a manageable safety profile.

This study evaluates the novel, chemotherapy-free combination of PI3Ki copanlisib and BCL2i venetoclax as a new targeted therapy for patients with relapsed/refractory mantle cell lymphoma.

Adding venetoclax to RBAC chemo-immunotherapy improves 2-year progression-free survival to 60% for older, high-risk MCL patients, validating a new risk-stratified, fixed-duration frontline treatment.

This phase II trial protocol compares chemo-free ibrutinib/venetoclax/rituximab versus ibrutinib-chemoimmunotherapy in treatment-naive elderly MCL, aiming to establish a new frontline standard.

Genomic analysis of MCL treated sequentially with BTKi and venetoclax identifies specific copy number alterations (e.g., 9p21.3 deletion) as novel biomarkers for primary and acquired resistance.

This phase 1 study shows the novel chemo-free triplet of magrolimab (anti-CD47), obinutuzumab, and venetoclax is a potential strategy for relapsed/refractory B-cell lymphomas, including MCL.

The combination of ibrutinib and venetoclax improves progression-free survival in relapsed/refractory MCL, establishing a highly effective, chemotherapy-free regimen for this difficult-to-treat population.

This preclinical study demonstrates potent anti-MCL activity with a triple combination of bendamustine, acalabrutinib, and venetoclax, providing a strong rationale for future clinical trials.

In high-risk, relapsed/refractory MCL, real-world data shows BTKi plus venetoclax is highly effective, with no added survival benefit from an anti-CD20 monoclonal antibody.

This review outlines emerging therapeutic strategies, including non-covalent BTKis, CAR-T, and bispecifics, for managing the clinically challenging population of MCL patients relapsing after covalent BTK inhibitors.

This review summarizes current and emerging therapies for relapsed/refractory MCL, highlighting key strategies like BTKi/BCL2i combinations, CAR-T, and bispecific antibodies for this poor-prognosis population.

In relapsed/refractory MCL, the phase 3 SYMPATICO trial established ibrutinib plus venetoclax as superior to ibrutinib alone, significantly improving median progression-free survival by nearly 10 months.

The chemotherapy-free BOVen regimen (zanubrutinib, obinutuzumab, venetoclax) shows high efficacy (88% CR) and deep MRD negativity in previously untreated, high-risk TP53-mutated MCL, a historically chemo-refractory population.

This CLL study reveals venetoclax rapidly activates a BAFF-driven survival axis in residual tumor cells, a key resistance mechanism potentially targetable in MCL to deepen BCL2i responses.

Reviewing AIM and SYMPATICO trials, the ibrutinib-venetoclax combination shows high efficacy in relapsed/refractory MCL, supporting a potential fixed-duration, MRD-guided treatment strategy.

In preclinical models, PTEN loss activates the PI3K/AKT pathway, reducing BCR signaling dependence and conferring resistance to ibrutinib, venetoclax, and PI3K inhibitors, identifying a key resistance mechanism.

The VALERIA trial demonstrates that an MRD-guided, fixed-duration venetoclax-lenalidomide-rituximab regimen is a highly effective, personalized, chemotherapy-free strategy for patients with relapsed/refractory MCL.

The frontline, chemotherapy-free triplet of acalabrutinib, venetoclax, and rituximab achieved 100% ORR and high MRD negativity, establishing a potent, time-limited option despite significant COVID-19 toxicity.

This review synthesizes current and emerging therapies for relapsed/refractory MCL, including BTKi, BCL2i, CAR-T, and bispecifics, emphasizing the evolving challenge of post-BTKi treatment sequencing.

Seven-year follow-up of venetoclax-ibrutinib in relapsed/refractory MCL shows durable responses (30% PFS) and demonstrates feasibility of MRD-guided treatment-free remission, supporting a long-term chemotherapy-free strategy.

Preclinical data shows the novel CTPS1 inhibitor STP-B has single-agent activity in high-risk MCL (blastoid, TP53-mutated) and synergizes with venetoclax by downregulating MCL1, offering a new combination strategy.

This review summarizes the evolving treatment landscape for relapsed/refractory MCL, highlighting survival gains from BTKi and CAR-T and outlining emerging therapies like bispecifics for multiply-refractory patients.